Professor Ron Davis's response to Naviaux study, including Q and A with Dr Naviaux

[msf]

Of course, the guy is incredibly overworked and this was just his first reaction to it, so perhaps he will change his mind on this.

 

[msf]

Finally, Prof. Davis also fails to distinguish between the reasons people with ME take antimicrobials. If people are taking antimicrobials just because they have a hunch that ME is caused by persistent infection, then I think that this study neither establishes or destroys the rational (or irrational) basis for such treatment. But what if they, for instance, have evidence of active infection? Many do, and many have equivocal evidence for such. Also, what if they are taking antimicrobials for gut dysbiosis/SIBO? Since the microbiome was one of the factors they identified in the study, it would seem a bit early to rule out things like Rifaximin.

 

[Fighttolive]

Here is my guess, though they can speak for themselves.

MS is a clear immune assault. Symptomatically its similar, but at this point we have no good grounds, that I am aware of, to presume its metabolic profile is similar.

Alterations in biological adaptation exist within medicine, and include depression. Its possible a subset of depression may have similar biochemistry, and that is important to know. Even if it does, however, that does not mean ME or CFS is depression. It might, for example, mean these patients who are classified as having depression actually have something else, and they need to be removed from the depression classification. What that will do however is decrease the specificity of the diagnostic test, though after investigation it might turn out these depressed patients do have ME or something similar and are being misdiagnosed.

PTSD is less clear. That does baffle me a bit. It is however an acute brain response to overwhelming stimuli, with long term changes to the brain. It is not clear there are long term metabolic changes, but its an intriguing question.

This is not about looking at similar symptomology ... its more about looking at potentially similar metabolism. The more separable you can show the test to be, the better.

I have to say I started feeling off after a severe 2 months of anxiety, with chronic hyperventilation daily, constantly. Initially maybe I thought I could have poisoned myself somehow with C02, hypoxia or whatever. I would be very intrigued to see how psychological stress could trigger this response, if it's considered a threat, it makes sense. I do have "PTSD"

 

[Ben H]

Finally, Prof. Davis also fails to distinguish between the reasons people with ME take antimicrobials. If people are taking antimicrobials just because they have a hunch that ME is caused by persistent infection, then I think that this study neither establishes or destroys the rational (or irrational) basis for such treatment. But what if they, for instance, have evidence of active infection? Many do, and many have equivocal evidence for such. Also, what if they are taking antimicrobials for gut dysbiosis/SIBO? Since the microbiome was one of the factors they identified in the study, it would seem a bit early to rule out things like Rifaximin.

Hi @msf

Many of us have had elevated viral titres, some elevated elispot's etc and have no such luck with extensive antivirals or abx. And to the contrary have been made worse. Not just on the basis of a 'hunch' but specific, targeted therapy based on lab results.

I think Prof. Davis is clearly aware of the reasons people take antimicrobials. Not sure where you are getting the idea that he isn't aware from...



B

 

[msf]

So why conflate them all? Because you are overworked? If so, fair enough.

And when I talked about evidence for active infection, I wasn´t talking about the things you mentioned. I meant things that would qualify someone as actively infected in any practice in any western country. I would put the stuff you mentioned in the category of equivocal evidence.

Also, the fact that antimicrobials didn´t help someone doesn´t necessarily mean that they don´t have an infection.

 

[Ben H]

Prof. Davis is extremely meticulous, and does not say things without good reason. Certainly not due to being overworked, or any other reason. He is a man of science. I won't wax lyrical, just take a look at his career thus far.

I think it best we wait for his possible response before assumptions are made on behalf of Prof. Davis


B

 

[msf]

I thought we did? Or do you mean his response to my response to his response to the study? I don´t think my concerns merit that, I would rather he just had a good chat with Naviaux about the significance of the study sometime.

 

[snowathlete]

Now that a collective understanding is being reached on the forum that the issue is a signaling problem that is stuck, I want to bring to attention the occurrence of spontaneous remission and relapse that repeats itself in some cases. How are these two things possible? If it is an evolutionary adaptive signal that is for our protection, how could it ever spontaneously shut off and on? How could it both be working correctly and malfunctioning?

This condition is so much more complex than everyone realizes. It requires a complete paradigm shift in order to begin to grasp it. It has to be turned from a two dimensional problem to a three dimensional one, and in order to do that the subconscious mind has to be introduced into the equation.

People also have different onsets. Many have sudden onset. Some have gradual onset, and some like me have a bit of both. Mine was gradual over many years, perhaps more than a decade, up and down, and then, at the end leading up to my diagnosis, a very sudden onset that left me permanently sick. I've often wondered about this. It may be that some signals in the body are in conflict, cancelling each other out partially and to varying degrees, and illness being where the CDR signalling is much more on. This might also explain remissions, that something changes the balance resulting in a remission where normal signals are much stronger. I don't know if this is possible, but if it is at a cellular level with mitochondria playing a key role then who is to say all of them are sending out the same signals?

 

[snowathlete]

I thought we did? Or do you mean his response to my response to his response to the study? I don´t think my concerns merit that, I would prefer that he just have a good chat with Naviaux about the significance of the study sometime.

Davis edited Naviaux's paper, and they are both part of the OMF so I'm sure they've both had plenty of good chats to be fair.

 

[lansbergen]

subconscious mind has to be introduced into the equation.

What is the subconscious mind?

 

[msf]

Davis edited Naviaux's paper, and they are both part of the OMF so I'm sure they've both had plenty of good chats to be fair.

Alright, I will leave it at that. I think Naviaux´s conclusions are more reasonable, for the reasons I gave above.

 

[Janet Dafoe]

The quote Halycon posted earlier in the thread indicates that Naviaux doesn´t agree with you.

Anyway, I didn´t want to make this thread a re-hash of all the chronic infection threads, I just wanted to point out that, in my opinion, it wasn´t reasonable to draw the conclusion that Davis drew from this study, and that Naviaux´s interpretation was much more reasonable.

Davis and Naviaux do not disagree with each other. They talk almost every day. I'm not sure what the science is here. I will ask Ron to clarify.

 

[cmt12]

Last post then I'm done

It may be that some signals in the body are in conflict

I do understand this to be the case, but I do not believe it is an error. I don't believe that the signaling mechanism is capable of signaling a return to equilibrium while the body is stuck in a hyper state. What it can do, however, is signal for a hypo state. So, it is a hypo state layered on top of a hyper state. Researchers can only see the top layer, which is the hypo state.

To understand the entire picture, you have to look at it in terms of depth and layering. Normally, what happens is a stressor induces a hyper state, and then the mechanism buries/stores the hyper state which allows the body to go back to baseline. When there is no more ability to bury and hide these hyper states (overflow), then the only option to get rid of the hyper state is to cover it with a hypo state. This is long term ME/CFS.

Spontaneous relapses and remissions are when you are bordering on the limit of what can be buried/stored. People who go from hyper state when stressed back to normal ("healthy people") still have enough "space" to use up for hiding and storing.

Why are these hyper, stressed states stored? It's so that every generation doesn't have to relearn the stressors of previous generations. They are stored and passed on.

 

[Janet Dafoe]

I thought we did? Or do you mean his response to my response to his response to the study? I don´t think my concerns merit that, I would rather he just had a good chat with Naviaux about the significance of the study sometime.

Ron and Bob have extensive "chats" almost daily. You are assuming things not in evidence. I will try to get Ron to clarify this point as soon as I can.

 

[Research 1st]

Finally, Prof. Davis also fails to distinguish between the reasons people with ME take antimicrobials. If people are taking antimicrobials just because they have a hunch that ME is caused by persistent infection, then I think that this study neither establishes or destroys the rational (or irrational) basis for such treatment. But what if they, for instance, have evidence of active infection? Many do, and many have equivocal evidence for such. Also, what if they are taking antimicrobials for gut dysbiosis/SIBO? Since the microbiome was one of the factors they identified in the study, it would seem a bit early to rule out things like Rifaximin.

These are fair points and worth raising for discussion, so I hope you don't mind. Relatively recently, researcher physicians like KDM in Europe have made some fascinating discoveries in PWME he sees, such as:

+Elevated D-Lactate (stomach bacterial overgrowth)
+Elevated Ammonia - Going down the Lyme route again.
+Kyneurenic Acid elevation - associated to Quinolinic acid, itself a neurotoxin - known to be elevated in neuro diseases, cancer and autoimmune diseases. Inflammation also is present (discussed later).

In addition to the above stool tests in many of KDM's 'ME' patients, and including people on this forum (who test of course) find they have overgrowth of certain bacterias that all correlate with the above 'phenomena' including the development of allergy syndromes from 'leaky gut', which until tests were developed, no one believed was possible.

All of this isn't mainstream, and it's probably quite rare that the 'average Joe' in the CFS community is even ware of this, primarily as 'infected people' with ME CFS, tend to hang out with the Chronic Lyme crowd, as they have Borrelia and other associated infections (Chlamydia Pneumonia Bartonela, Babesia etc) and the 'CFS' patients tend not to test, or are too ill or have no funds to. Hence we have the split, in opinion about CFS vs Chronic Lyme and will never agree with each other until robust tests are developed for both conditions.

KDM's fingerprints of chronic intracellular infections discovered in his ME patients are coupled with existing knowledge and evidence of inflammatory markers which then correlate with a state of chronic, re-activated, or even latent activated infections:

+PGE2
+Cytokines and Chemokines
(I would add: LDH, HS-CRP, Blood Viscocity (better than ESR which tends to be neg in ME) into the mix here personally and not even bother with CRP/ESR as it's usually normal - hence the misdiagnosis of 'no inflammation'.

Infections such as Bartonella can infected endothelium and infections can screw up blood flow and lower oxygen utilization (hypoxia). Again, inflammation is indicated once more:

+VEGF
+TGF-B1
+VIP

And Molds. Mold overgrowth is common in people with immune suppression. PW immune suppression report more incident of infections - what some PWME report they now have, others report they are never infected and rarely even get a cold - are these the people we are hearing about from researchers who test negative all the time? It would seem so. Did they also test the above markers in bold I have listed? I would imagine not. It all costs money.

Now you could argue, that none of these people with 'infections' have ME CFS, they have Lyme. But we are told by officials Chronic Lyme doesn't exist and people have psychogenic PTLDS, a silly idea that infections are incapable of being chronic, in illnesses we don't understand.

With this Mito technology, when available, patients with all sorts of conditions from ME, CFS POTS, Lyme, MS, Autism, etc can in the future, test themselves if they wish, and see if they have ''the CFS defect'', now if they do, and don't have ''CFS''' diagnosis, that will be most interesting as it implies that the core cause behind multiple allied syndromes, has been missed - e.g. a Virus, Bacteria, Retrovirus etc.

Finally over the next few years we can all come together as patients (potentially to find out) 3 final outcomes:

1) Chronic Lyme is CFS and unrelated to classical Borrelia Infection.
or
2)Chronic Lyme is another disease entirely, causing chronic infections and people were all misdiagnosed with CFS.
or
3) Chronic Lyme isn't CFS , but requires the Mito 'CFS defect' (discussed in this thread) leading to a state of Chronic Lyme only possible *due to having ME CFS* as it causes a new form of immune suppression, which itself may then leads to autoimmunity and HERV activation, perhaps, not seen in CFS alone.

I think we all have biases, it's only human nature and that includes researchers 'on our side'.

If we are experts in: Mito, Viruses, Bacteria, Autoimmune....

We'll all focus on our specific field, and carry these beliefs with us that 'this' must be the cause. Patients do the same, because we test ourselves and find bugs, or we find nothing, or we find autoimmunity and no bugs, or both! So we're all set on certain paths to a degree, even if we are careful to be as open minded as possible.

This shouldn't be a problem in the future, with the control of the Government BPS theory of CFS out of the way *due to private research funding at the OMF allowing for this bypass* of irrational science - Science based on self reported fatigue. (Crazy idea to discover diseases).

It's probably fair to say the whole theory of ME will be unified in the future anyway, and everyone will be 'right' to a degree (e.g. many defects will be found from various fields of Science) and the differences that will remain are observed due to subsets of disease, and patients having completely unique presentations, within those subsets.

I would hazard a guess the infected people with CFS/Lyme are more 'visibly sick' to doctors (raised lymph glands, development of Asthma, Cancer etc), than those crippled in bed by raw ME extreme exhaustion. Visibly ill patients can 'justify' to a doctor they need complex costly tests, and get tested and hey presto, 5 infections show up in some subsets.

Conversely if you're laying in bed and can't speak or move, the average patient won't be able to tolerate/afford, endless blood draws to find a certain pathogen and thus themselves or their careers won't believe an chronic infection causes their disease at all.

Hence in summary, this is probably why each group of biomedical CFS researcher has their own beliefs, because of who they see in clinic, or what type of patient their blood, saliva, stool samples are analyzed from.

Currently with no test, there are many reasons for being housebound or bedridden and they don't have to be Infectious, Autoimmune, Mito, and can indeed be psychosomatic. It's just luck (due to no test) which research group gets which kind of blood sample - hence the differences in research conclusions.

A good example of this is 85% of blood samples from Dr Montoya's group had retroviruses (data never made public due to political censorship), and another CF clinic who gave samples in, Dr Bateman's I believe, has 0%. Why the difference? Because people who go to see Dr Montoya are more likely to have infections, as he's a specialist in this area not 'fatigue'. Arguably, his patients are more sick, so statistically they are more likely to be infected with a pathogen and have high cytokine levels also. The worrying aspect for us, is both pools of patient samples carry a diagnosis of CFS - with opposing results.

There is no way to stop this, unless you spend hours with the patient (or carers) going through medical histories, which is impossible if you need to sample 500 blood tubes from 'CFS' patients with tiny budgets and time constraints and few staff.

With a Mito test, you begin to say, OK, if this person has this, either they have it or they don't. Only then can we agree or dismiss pathogen association to CFS, and if it's not present, the infected patients have another condition such as ME/Lyme. Which makes things even more complicated as we are all told ME is CFS.

We'll have to wait and see.

 

[alex3619]

Now that a collective understanding is being reached on the forum that the issue is a signaling problem that is stuck, I want to bring to attention the occurrence of spontaneous remission and relapse that repeats itself in some cases. How are these two things possible? If it is an evolutionary adaptive signal that is for our protection, how could it ever spontaneously shut off and on? How could it both be working correctly and malfunctioning?

This condition is so much more complex than everyone realizes. It requires a complete paradigm shift in order to begin to grasp it. It has to be turned from a two dimensional problem to a three dimensional one, and in order to do that the subconscious mind has to be introduced into the equation.

Subconscious mind is an unproven, hypothetical, construct. It does not have to be considered anywhere, and I would prefer if it were completely eradicated from evidence based medicine. As an hypothetical area of research it is fine. I personally think the term "subconscious" has long outlived its usefulness, as has "mind". My left little toe nail is often outside my conscious awareness. So what?

We have not reached a consensus that a signalling issue is stuck. We are moving to understanding the current research, and new research findings will change our views again.

How could it shut off? Its an enforced state if the current interpretation is correct. So if the signals are temporarily stopped, or opposed, or the stop trigger is sent ... instant temporary or long term remission. This is totally within the implications of the current research. In fact it explains remissions ... but nothing yet has proved this idea of a stuck signal. Its just a strong hypothesis, and we are eager to see it tested.

The condition is indeed complex. The function of brain and other communications mechanisms (command and control includes metabolites, hormones - and not just endocrine hormones - the immune system, central and peripheral neurological systems and so on) are routinely ignored in research that cites the subconscious, though not by everyone, especially neurologists. The claims to subconscious cause for disease have, in the history of medicine, never been proved, though they are often cited. They have, repeatedly, been completely disproved. This is religion and pseudoscience, not science, if its claimed as fact or scientific. As unproven hypothesis its fine. It has no place in clinical medicine. If you think any disease state has been proven to be driven by the subconscious, thoroughly, with replicated research, please cite the most important study. I have never seen anyone able to do that, though they often respond by citing junk and irrelevant studies.

 

[alex3619]

who is to say all of them are sending out the same signals?

They wont be. Its about net signals impacting on critical systems. I have previously discussed this in terms of waves, which can reinforce or cancel each other out. I could also discuss this in terms of neural signalling, though its not nearly that simple for either analogy.

 

[msf]

Oh no, someone mentioned Lyme. I purposefully kept my objections as general as possible, because I didn´t want it turning into another Lyme thread.

 

[lansbergen]

What it can do, however, is signal for a hypo state. So, it is a hypo state layered on top of a hyper state.

I like that.

 

[Cheshire]

What is the subconscious mind?

Something very convenient that can fill nearly any gap?